The aim of this project is to identify changes in membrane trafficking, resulting from the disruption of microtubule-based motility in lacrimal acinar gland cells. Microtubules (MTs) are ubiquitous constituents of eukaryotic cells and serve a variety of functions, such as membrane trafficking, endocytosis, and secretion. It is our hypothesis that MTs facilitate stimulated secretion in lacrimal acini by supporting movement of secretory vesicles to the apical plasma membrane (APM). This MT-based transport could be facilitated by cytoplasmic dynein, a minus-end directed MT-motor protein. We will test this hypothesis by introducing function-blocking antibodies into the acini and analyzing the changes in membrane traffic by confocal fluorescence and electron microscopy. It is hoped that elucidating basic features by lacrimal gland physiology will facilitate a better understanding of the mechanism underlying lacrimal insufficiency, a major contributor to ocular morbidity.